Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of prior glycogen depletion on glycolysis [flux through phosphofructokinase (PFK)] and inosine monophosphate (IMP) formation in human skeletal muscle has been investigated. Eight subjects cycled at a work load calculated to elicit 95% of maximal O2 uptake on two occasions, the first to fatigue [5.5 +/- 0.3 (SE) min] and the second at the same workload and for the same duration as the first. Before the first experiment, muscle glycogen stores were lowered by a combination of exercise and diet. Before the second experiment, muscle glycogen stores were supercompensated. In the low-glycogen (LG) state muscle glycogen decreased from 201 +/- 31 mmol glucosyl units/kg dry wt at rest to 105 +/- 28 after exercise, and in the high-glycogen (HG) state from 583 +/- 40 to 460 +/- 49. The accumulation of fructose 6-phosphate (F-6-P; activator of PFK) during exercise was markedly attenuated in the LG state (P less than 0.01), whereas lactate accumulation in muscle was similar between treatments, suggesting that muscle pH was also similar. Glycolysis (estimated from glycogenolysis minus accumulation of hexose monophosphates) was not measurably different between treatments (LG = 88 +/- 17, HG = 106 +/- 43 mmol/kg dry wt; P greater than 0.05). IMP was significantly greater in the LG state after exercise (3.63 +/- 0.85 vs. 1.97 +/- 0.44 mmol/kg dry wt; P less than 0.05). It is concluded that decreased glycogen availability does not measurably alter the rate of muscle glycolysis during intense exercise. It is hypothesized that the attenuated increase in F-6-P in the LG state, which should theoretically decrease glycolysis, is compensated for by increases in free ADP and AMP (activators of PFK) at the enzymatic site during the contraction phase. The greater increase in IMP in the LG state is consistent with this hypothesis, since ADP and AMP are also activators of AMP deaminase.
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PMID:Role of glycogen in control of glycolysis and IMP formation in human muscle during exercise. 205 62

In E. coli WP2 trpE65 cells irradiated with UV-dose of 11 J/m2, the additional small portion of induced Trp+ mutations became resistant to photoreactivation or "dark" (excision) repair after a short-termed (10-30 min) postirradiation incubation of bacteria in a minimal medium deprived of glucose and tryptophan. Since protein synthesis could not proceed in those cells because of the lack of energy and tryptophan, the data indicate that an unknown mechanism exists which imparts some mutations with the resistance to antimutagenic repair in the absence of the inducible mutagenic system. In the light of this result, one could suggest that the normal process of mutation fixation (that is the loss of sensitivity of mutations to photoreactivation or to excision repair in cells incubated in growth medium after irradiation) should not necessarily be a direct consequence of manifestation of the activity of an inducible mutagenic system.
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PMID:[Increase in the fraction of non-repaired mutations in Escherichia coli cells, incubated in the absence of glucose after UV-irradiation]. 207 11

This paper reports the effect of endurance exercise training on bicycle ergometer by interval method (work and interval each 1:1 min) and continuous method on increase of physical performance, decrease of heart rate, rate-pressure-product, glucose, lactate, and catecholamines. Two groups of nine male patients (aged 59 +/- 4 vs 56 +/- 6 (mean +/- SD)) after coronary bypass surgery each participated in the inpatient rehabilitation training. Training started 24 and 26 days, resp., after surgery and lasted for 3.5 weeks. Frequency and duration of exercise training: Monday-Friday 1 x 20 min and 1 x 25 min per day; Saturday/Sunday each 1 x 25 min per day. In the interval group and the continuous group the exercise training intensity was set at 86% of individual max. heart rate. In the last week of training mean exercise intensity was at 83 watts in the group of patients who were trained by the continuous method and at 20:121 watts in the group of patients who were trained by the interval method. Before and after the training period patients underwent a multistage bicycle ergometer exercise test in sitting position. Beginning at 25 w, each stage was increased by 25 w, whereby each stage lasted 3 min. Cutoff criteria were heart rate (220 - age x 0.85) and/or fatigue of the leg muscles.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of interval versus endurance training of increasing performance, cardiovascular function, metabolism and catecholamines in selected patients after aortocoronary bypass operation]. 208 57

Skeletal muscle, liver and heart glycogen variations, induced by swimming in thermal water (at 35 degrees C) as a model of physical exercise for clinical use, were studied. Muscle and liver glycogen moderately decreases after a 30-min period of swimming and comes near to depletion after 60 min. Heart glycogen decreases only slightly after 60 min. Blood glucose and plasma insulin decrease only after 60 min of swimming. A 30-min swim in thermal water, cooled to 25 degrees C, depletes muscle and liver glycogen and slightly decreases heart glycogen. Under these conditions, plasma insulin decreases and hypoglycemia occurs. The results seem to indicate some advantages of swimming in hot thermal water in order to prevent glycogen store depletion as the physiological prerequisite for a physical exercise of clinical interest to obtain therapeutical benefits, avoiding premature fatigue and exhaustion.
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PMID:Effect of swimming in thermal water on skeletal muscle, liver and heart glycogen. 213 67

Maintenance of low coronary flow (1 ml/min) during 40 or 70 min of anoxia maintained function and prevented Ca2+ overload during reoxygenation in isolated rat hearts. In comparison, recovery from 40 min of global ischemia resulted in only 20% of preischemic function and an increase in end-diastolic pressure (LVEDP) to 39 mmHg. Reperfusion Ca2+ uptake rose from 0.6 to 10.2 mumol/g dry tissue. Intracellular Na+ (Nai+) increased from 13 to 61 mumol/g dry tissue after 40 min of global ischemia, but was unchanged in hearts with low flow anoxia. When glucose and pyruvate were omitted from buffer used for anoxic perfusion, recovery was only 15% of preanoxic values, LVEDP rose to 32 mmHg, and reperfusion Ca2+ uptake was 7.2 mumol/g dry. In addition, Nai+ increased (47.4 mumol/g dry tissue) and ATP was depleted (1.0 mumol/g dry tissue) in the absence of substrate. In anoxic hearts supplied substrate, Nai+ stayed low (12 mumol/g dry tissue) and ATP was preserved (11.6 mumol/g dry tissue). Addition of ouabain (100 or 200 microM) and provision of zero-K+ buffer increased Nai+ and resulted in impaired functional recovery, increased LVEDP, and greater reperfusion Ca2+ uptake. These interventions also decreased energy availability in anoxic hearts. To distinguish between effects of Na+ accumulation and ATP depletion, monensin, a Na+ ionophore, was added during low flow anoxia. Monensin increased Nai+, decreased functional recovery and increased reperfusion Ca2+ uptake in a dose-dependent manner (1-10 microM) without changing ATP content. These results suggested that reduction of Nai+ accumulation by maintenance of Na+, K+ pump activity was the major mechanism of the beneficial effects of low coronary flow on reperfusion injury.
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PMID:Na+ accumulation increases Ca2+ overload and impairs function in anoxic rat heart. 215 54

A 31-year-old male patient with type Ia glycogen storage disease was admitted to our department complaining of general fatigue and right hypochondriac pain. He exhibited massive hepatomegaly with systemic hypoglycemia, lactic acidosis, hyperuricemia, hyperpyruvatemia and hyperlipemia. The failure of blood glucose levels to increase after a glucagon loading test, and a reduced lactate level on glucose tolerance test were also observed. Various imaging techniques suggested hepatic adenoma with hemorrhage in the tumor, which was confirmed histologically. There was a complete absence of glucose 6-phosphatase activity, as determined by an enzyme assay on resected liver specimens, which proved the case to be type Ia glycogen storage disease. We also reviewed all previously reported cases of hepatic tumor and glycogen storage diseases. We conclude that, since hepatic adenoma is not rare in this disease, and is complicated by hemorrhage, rupture and malignancy, careful follow-ups are necessary.
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PMID:A case of type Ia glycogen storage disease complicated by hepatic adenoma. 217 Feb 59

Substrate depletion and end product accumulation are two important factors in exercise fatigue. Fatigue during long-term exercise results from a depletion of muscle and liver glycogen and coincides with an inability to maintain blood glucose levels. During high intensity exercise, the rapid catabolism of carbohydrate and the resultant production of lactate and hydrogen ions cause a reduction in muscle pH that inhibits maximum force generation. Dietary manipulations that can influence carbohydrate status or lactate accumulation may be beneficial to performance. In human athletes, carbohydrate loading and carbohydrate supplementation can enhance endurance time during long-term exercise. These practices have not been explored extensively in the equine athlete, although glycogen loading does not enhance the performance of horses during short-term intense work. Short-term work can be detrimentally affected if glycogen levels are inadequate. The most marked effect of exercise on nutrient requirements is in the energy requirement. Horses in heavy training may require more energy than they can consume on a conventional diet. Fat has been added to horse diets to increase energy density, usually at levels between 6% and 12% of the total diet. Although protein requirements may be slightly increased in the working horse, supplementing protein as a means of adding calories is not an efficient practice. In addition, although studies with horses are not available, human studies indicate that there are no benefits to vitamin supplementation above required levels. At this point, more is unknown than is known about feeding performance horses. Most information on fuel utilization is extrapolated from studies with rats and humans. Areas that have received little attention but are critical to optimizing feeding practices are the timing of pre-event feeding and the determination of ideal body composition in equine athletes of different types.
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PMID:Nutrition and fuel utilization in the athletic horse. 220 99

The diabetic hypersomolar state is defined by a serum glucose greater than 600 mg/dl and a serum osmolarity greater than 320 m Osm/L. Ketoacidosis or lactic acidosis may co-exist with DHS in the same patient. The incidence of this acute complication of diabetes is high enough (17.5 cases per 100,000 person-years) for primary care physicians to encounter a case every year or two. Predisposing factors include older age, female sex, nursing home residence, and infection. A substantial proportion of cases occur in patients with no prior history of diabetes. Common presenting signs include fatigue or weakness, polydipsia, polyuria, nausea, and alteration of consciousness. The mainstay of therapy is intravenous fluid replacement with close monitoring of glucose and electrolytes in a hospital setting. Current mortality figures are high, at 10% to 20%, and the chance of survival is adversely affected by older age, higher osmolarity, and the presence of an associated severe illness. Prevention includes screening for diabetes, educating diabetic patients and their care givers about the symptoms of hyperglycemia, prompt treatment of any infection in a diabetic person, avoidance of drugs that increase carbohydrate intolerance in diabetic people, and encouraging compliance with treatment of diabetes.
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PMID:The diabetic hyperosmolar state. 222 47

Inhibition of hepatic long chain fatty acid oxidation by 2-5-4 chlorophenylpentyloxirane-2-carboxylate (POCA) leads to decreased gluconeogenic rates from lactate or from low concentrations of pyruvate. The inhibitory effect is fully overcome by concentrations of pyruvate above 0.8 mM or by the simultaneous administration of a medium chain fatty acid. At low pyruvate availability the energy cost of gluconeogenesis is mainly supported by fatty acid oxidation and POCA-induced inhibition of glucose production is secondary to a decreased energy availability. This is supported by the following observations: (i) POCA decreases hepatic respiration and phosphorylation potential: (ii) the rate of pyruvate-induced respiration was the same regardless of whether gluconeogenesis was inhibited or not by POCA: and (iii) concentrations of pyruvate above 0.8 mM, at which gluconeogenesis is not inhibited, prevented the POCA-induced decrease in the phosphorylation potential. It is concluded that inhibition of long chain fatty acid oxidation by POCA leads to a switch of energy fuel, and results in the oxidation of more pyruvate to meet the cellular energy demands. When pyruvate availability is low and thus, presumably, its mitochondrial transport restricted, pyruvate carboxylation most probably becomes limiting as a result of the increased flux through pyruvate dehydrogenase, in the presence of POCA.
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PMID:On the mechanism of sodium 2-5-4 chlorophenylpentyloxirane-2-carboxylate (POCA) inhibition of hepatic gluconeogenesis. 224 6

Numerous studies report controversial results about the occurrence and role of cardiodepressant substances in various forms of circulatory shock. We investigated the net inotropic effect of the low molecular weight fraction (mol wt less than or equal to 1,000) of plasma in prolonged canine hypovolemic traumatic shock using an in vitro guinea pig papillary muscle assay (isotonic mode). The shock plasma fractions (ultrafiltrates) after 4 hr of hypotension (mean arterial blood pressure 40-50 mm Hg) and immediately post-reinfusion significantly depressed papillary muscle function (P less than .02). The extent of papillary muscle shortening was decreased by 49.5 +/- 9.9% in pre- and 50.6 +/- 10.0% in post-reinfusion plasma ultrafiltrates (mean values +/- standard error of the mean; n = 6 shock experiments). In contrast, both the plasma ultrafiltrates from ten non-anesthetized healthy dogs and the control ultrafiltrates obtained prior to onset of shock in the experiments (-6.4 +/- 2.6; n = 6) induced no significant change of the in vitro performance of papillary muscle contraction. These results were achieved with plasma fractions in which ionized calcium and pH were adjusted to concentrations equivalent to the bioassay solution. Lactate acidosis and severe hypoglycemia (1.97 +/- 0.43 mM post-reinfusion) occurred in the shock experiments. Lack of energy substrate (glucose) was not responsible for the in vitro depression. Four depressive shock ultrafiltrates with glucose concentrations adjusted to control ultrafiltrate levels induced a 66.6 +/- 8.8% decrease in the extent of papillary muscle shortening. These results suggest that the possible occurrence of high net negative inotropic activity in plasma, especially just post-reinfusion, may play a role in the pathogenesis of irreversible circulatory shock.
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PMID:Net inotropic plasma activity in canine hypovolemic traumatic shock: low molecular weight plasma fraction after prolonged hypotension depresses cardiac muscle performance in vitro. 231 Dec 3


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